Deprenyl (also referred to herein as selegiline or R-(−)-N, α-Dimethyl-N-2-propynyl phenethylamine) was first used as an adjunct to conventional drug therapy (L-dihydroxyphenylalanine (L-DOPA) plus a peripheral decarboxylase inhibitor) of Parkinson's disease (PD) in Europe over a decade ago on the basis that as a selective monoamine oxidase-B (MAO-B) inhibitor, it would elevate brain dopamine levels and potentiate the pharmacologic action of dopamine formed from L-DOPA, and yet prevent the tyramine-pressor effect observed with non-selective MAO inhibitors. The combined drug therapy was reported to prolong the anti-akinetic effects of L-DOPA, resulting in the disappearance of on-off effects, reduced functional disability, and increased life-expectancy in PD patients (Bernheimer, H., et al., J. Neurolog. Sci., 1973. 20: 415–455, Birkmayer, W., et al., J. Neural Transm., 1975. 36:303–336, Birkmayer, W., et al., Mod. Prob. Pharmacopsychiatr., 1983. 19: 170–177, Birkmayer, W. and P. Riederer, Hassler, R. G. and J. F. Christ (Ed.) Advances In Neurology, 1984. 40(Y): p. 0–89004, and Birkmayer, W., et al., J. Neural Transm., 1985. 64(2): p. 113–128).
Studies examining deprenyl as an adjunct to conventional L-DOPA therapy have reported a short term benefit which was usually lost by 1 year or less. Some, but not all, have reported that the levodopa dose can be decreased when taken in conjunction with deprenyl (Elizan, T. S., et al., Arch Neurol, 1989. 46(12): p. 1280–1283, Fischer, P.A. and H. Baas, J. Neural Transm. (suppl.), 1987.25: p. 137–147, Golbe, L. I., Neurology, 1989.39: p. 1109–1111, Lieberman, A. N. et al., N.Y. State J. Med., 1987. 87: p. 646–649, Poewe, W., F. Gerstenbrand, and G. Ransomayr, J. Neural Transm. (suppl.), 1987. 25: p. 137–147, Cedarbaum, J. M., M. Hoey, and F. H. McDowell, J. Neurol. Neurosurg. Psychiatry, 1989. 52(2): p. 207–212, and Golbe, L. I., J. W. Langston, and I. Shoulson, Drugs, 1990. 39(5): p. 646–651).
Increasingly, deprenyl is being administered to Parkinson's disease patients following reports (Parkinson, S. G. Arch Neurol 46, 1052–1060 (1989) and U.S.A., Parkinson, S. G. N. Engl. J. Med. 321, 1364–1371 (1989)) that it delays the disease progression; a mechanism has recently been proposed to explain its action (See, e.g., Tatton & Redman 1996).
Peripheral neuropathy is art-recognized and is a common neurological disorder resulting from damage to the peripheral nerves. It is a condition which is associated with several underlying conditions, including conditions such as inheritable neuropathies, diabetes, rheumatoid arthritis, acquired immunodeficiency syndrome (AIDS) and thyroid disease or associated side-effect of anti-cancer therapy, i.e., cisplatin treatment (see J. Clinical Oncologyl4(6):1913 (1996), B. J Cancer 75(5):703 (1997) (for a review, see, e.g., Morgenlander, J.C., Postgrad. Med. (1997) 102 (3): 71, and references cited therein).
Peripheral neuropathies can be debilitating, and treatment of such neuropathies is often difficult. Accordingly, methods of inhibiting or preventing the progression of peripheral neuropathies are needed.